Although the neurotransmitter systems underlying the sedative subjective effects of alcohol have not been clearly characterized, there is some evidence that these effects are mediated by glutamatergic antagonism (Krystal et al., 1998). Likewise, the sedative and anxiolytic effects of alcohol, more prominent during the descending limb, are thought to be mediated by γ-Aminobutric Acid (GABA) neurotransmission (Buck, 1996; Grobin et al., 1998). As discussed above, understanding the substrates underlying subjective responses to alcohol has the potential to improve gene identification by focusing on a more narrowly defined and biologically-relevant phenotype. To that end, a number of genetic association studies have examined candidate genes for level of response to alcohol, as defined by Schuckit and colleagues (e.g., Schuckit & Smith, 1996; Schuckit et al., 1999). Results to date have not been entirely consistent, yet there is some support for the role of variation in the GABAAα6 and serotonin transporter in the subjective response to alcohol in the laboratory (Corbin, Fromme, and Bergenson, 2006; Fromme et al., 2004; Schuckit et al., 1999). In a recent review of the literature on genes contributing
